YI 04. Functional and Morphological Changes During Triggered Liver Regeneration


A Budai, A Fülöp, A. Szijártó, D. Korsós, L. Harsanyi, G. Lotz

Chair(s): Dávid Ágoston Kovács & Attila Szijárt (Moderator: Frank Dor)

9:00 - 9:10h at Erszebet Room (A)

Categories: Young Investigator Award, Hepatobiliary and Pancreatic Surgery

Session: Young Investigator Award


Invited discussant:
René Tolba, Nikolay Lvovich Matveev, Henrik Thorlacius, Ivo Post, Thomas Theologou, Ignacio Garcia Alonso


Background
Selective portal vein ligation (sPVL) results in ipsilateral atrophy and hypertrophy of contralateral liver segments. The aim of the present study was to examine the morphological and functional changes during this process.

Material and Methods
Male Wistar rats (n=84) underwent sPVL. The portal venous supply of the 80% of whole parenchyma was ligated. The regeneration rate, the lobular area and the portal pressure was measured. To quantify the mititoc and apoptotic activity Ki-67 and Caspase-3 immunostaining was performed. To measure the functional state of the liver indocyanine-green (ICG) clearance test was performed and the retention (R15) and the plasma disappearance rate (PDR) of the ICG was calculated. The animals were sacrificed 0, 12 hours, 1, 2, 3, 5, 7 days after sPVL.

Results
Liver regeneration rate was 266,2% at 7th postoperative days in lobes I-II and 18,8% in lobes III-VII. The mitotic activity reached its maximum 48h after sPVL (20.61 ± 3.56 vs. 142.33 ± 18.86). As a result of the upregulated cell division the lobular area significantly increased by the 7th postoperative day (300502,3789 ± 15402,38um2 vs. 714514,2965 ± 30490,89um2). According to the R15 and PDR scores the liver function temporarily impaired after the sPVL, and it increased parallel with the regeneration of the non-ligated lobes reaching the physiological level by 7th postoperative day.

Conclusion
According to our data it can be suggested that sPVL induced liver regeneration caused not only weight increase, but functional recovery as well.